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CompletedNCT02940327Mi-ECMOUpdated Mar 19, 2020Results posted

Markers of Inflammation and Lung Recovery in ECMO Patients for PPHN

An observational study in Persistent Pulmonary Hypertension of the Newborn, sponsored by University of Leicester. Completed at 1 site in United Kingdom. Open to participants aged Up to 30 Days. Per ClinicalTrials.gov, last updated 2020-03-19.

Sponsored by University of Leicester · Observational

Study type
Observational
Model
Case-control
Time perspective
Prospective
Enrollment
24
Ages
Up to 30 Days
Sex
All
01

Study summary

Respiratory failure in newborns is common and has high rates of death. Where conventional intensive care strategies have failed, newborn children are referred to treatment with Extra- Corporeal Membrane Oxygenation (ECMO). This involves connecting children via large bore cannulas placed in their heart and major blood vessels to an artificial lung that adds oxygen to their blood and removes waste gases (carbon dioxide). Although this treatment saves lives, it still has some limitations. In particular, severe complications like bleeding, or damage to the kidneys can occur. These complications can lead to death in some cases and long-term disability in others. Based on ongoing research in adults and children undergoing cardiac surgery the investigators have identified a new process that may underlie some of the complications observed in ECMO. The investigators have noted that when transfused blood is infused in an ECMO circuit, this results in the accelerated release of substances from the donor cells that cause organ damage; at least in adults. There are treatments that can reverse this process. Before the investigators explore whether these treatments should be used in newborn children on ECMO, the investigators must first demonstrate that they can measure the complex inflammatory processes that occur in these critically ill children. The investigators therefore propose to conduct a feasibility study to identify the practical issues and challenges that would need to be overcome in order to perform a successful trial in this high-risk population.

Read the detailed description

The primary hypothesis is that damage to red blood cells by the exposure to the ECMO circuit will result in inflammatory responses that mitigate against successful weaning from Extra-Corporeal Membrane Oxygenation (ECMO) for Persistent Pulmonary Hypertension of the Newborn (PPHN).

The secondary hypothesis are:

  1. Damage to red cells will result in platelet, leukocyte and endothelial activation.
  2. Markers of platelet, endothelial and leukocyte activation are indicators of lung inflammation and injury severity and hence lung recovery.
  3. Markers of platelet, endothelial and leukocyte activation are indicators of kidney injury severity and hence acute kidney injury.
  4. The level of oxidative stress will correlate with type shifts in pulmonary macrophages, tissue iron deposition and organ injury.
  5. Ability to raise anti-oxidative response, measured by Heme Oxigenase-1 (HMOX 1) expression, will correlate with shorter intubation times and less severe kidney and lung injury.
  6. Granulocyte and platelets activation are secondary to rising redox potential and the levels of activation will correlate with longer intubation times and more severe organ injury.
  7. Markers of anti-oxidative response, platelet, endothelial and leukocyte activation, as well as oxidative stress levels have diagnostic and prognostic utility for the prediction of key clinical events including delayed time to recovery, acute kidney injury in paediatric patients undergoing Extra-Corporeal Membrane Oxygenation (ECMO) for Persistent Pulmonary Hypertension of the Newborn (PPHN).

This is a pilot feasibility study that will establish the following:

  1. Recruitment rates and patient flows for 24 patients specified as the target population for the feasibility study
  2. Withdrawal rate, and completeness of follow-up and data collection in a paediatric population at high risk for death and major morbidity
  3. The proportions (categorical data) and variance (continuous data) for the primary and secondary outcomes of interest. These will be used to model the sample sizes and outcomes that may be used in a definitive study
  4. Perceptions of family members whose children participate in the study as to the appropriateness of the screening and consent process
02

Conditions studied

  • Persistent Pulmonary Hypertension of the Newborn

Keywords

  • ECMO
  • PPHN
  • Pulmonary Hypertension of the Newborn
  • Markers of inflammation
  • Mi-Ecmo
03

In context

Hypertension, Pulmonary

1,105 studies on the registry are indexed under Hypertension, Pulmonary; 234 are open to participants now.

This study's enrollment of 24 is below the median of 116 across 386 observational studies indexed under Hypertension, Pulmonary.

Browse Hypertension, Pulmonary studies →

Lead sponsor

University of Leicester is the lead sponsor of 166 studies on the registry; 51 are open to participants now.

Counted across the registry records on this site, refreshed daily.

04

Who can participate

Ages eligible
Up to 30 Days
Sexes eligible
All
Accepts healthy volunteers
No
Sampling method
Probability sample

Study population

The study will be conducted at a regional ECMO centre in the UK, the University Hospitals of Leicester NHS Trust. This unit performs over 60 neonatal and paediatric ECMO per year, of which at least 40 are expected to be performed for the treatment of PPHN in infants.

Inclusion criteria

  1. Patients with a diagnosis of PPHN
  2. Patients that require ECMO support as determined by the ECMO team
  3. Patients aged less than 30 days
  4. Emergency consent obtained within 12 hours from cannulation, and ultimately full consent

Exclusion criteria

Exclusion Criteria:

  1. PPHN is caused by a congenital heart pathology
  2. ECMO is required for a congenital heart disease
  3. Lack of consent
05

Study design

Observational model
Case-control
Time perspective
Prospective
Enrollment
24 participants (actual)
Patient registry
No
Biospecimen retention
Samples with dna
06

What researchers measure

Primary outcomes

  1. CD16/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 12 hours after ECMO commencement

  2. CD16/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 24 hours after ECMO commencement

  3. CD16/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 48 hours after ECMO commencement

  4. CD16/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 72 hours after ECMO commencement

  5. CD16/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 24 hours after decannulation

  6. CD14/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 12 hours after ECMO commencement

  7. CD14/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 24 hours after ECMO commencement

  8. CD14/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 48 hours after ECMO commencement

  9. CD14/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 72 hours after ECMO commencement

  10. CD14/41

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 24 hours after ECMO decannulation

  11. CD64/163

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 12 hours after ECMO commencement

  12. CD64/163

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 24 hours after ECMO commencement

  13. CD64/163

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 48 hours after ECMO commencement

  14. CD64/163

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 72 hours after ECMO commencement

  15. CD64/163

    Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

    Time frame: 24 hours after decannulation

Secondary outcomes

  1. Change of Serum Haemoglobin Levels

    Clinical and biochemical markers of organ failure

    Time frame: baseline

  2. Duration on ECMO

    Clinical and biochemical markers of organ failure

    Time frame: > 7 days or did not survive to discharge

  3. Number of Participants With Acute Kidney Injury

    Clinical and biochemical markers of organ failure

    Time frame: >7 days or did not survive to discharge

  4. Heart Injury as Determined by Serum Troponin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 12 hours after ECMO commencement

  5. Allogenic Red Cell Transfusion Volume

    Clinical and biochemical markers of organ failure

    Time frame: 24 hours after ECMO is discontinued

  6. Number of Participants Requiring Non Red Cell Transfusion

    Clinical and biochemical markers of organ failure

    Time frame: 24 hours after ECMO is discontinued

  7. Heart Injury as Determined by Serum Troponin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 24 hours after ECMO commencement

  8. Heart Injury as Determined by Serum Troponin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 48 hours after ECMO commencement

  9. Heart Injury as Determined by Serum Troponin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 72 hours after ECMO commencement

  10. Heart Injury as Determined by Serum Troponin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 24 hours after decannulation

  11. Change of Serum Haemoglobin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 12 hours after ECMO commencement

  12. Change of Serum Haemoglobin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 24 hours after ECMO commencement

  13. Change of Serum Haemoglobin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 48 hours after ECMO commencement

  14. Change of Serum Haemoglobin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 72 hours after ECMO commencement

  15. Change of Serum Haemoglobin Levels

    Clinical and biochemical markers of organ failure

    Time frame: 24 hours after decannulation

07

Results

Posted Mar 19, 2020

Participant flow

Participant flow — Overall Study
Milestone1 - Observational Case-Controls
Started24
Completed24
Not completed0

Outcome measures

PrimaryCD16/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
12 hours after ECMO commencement
Reported as:
Mean · percent change
CD16/41
percent change7+ Days<7 Days
CD16/411.90 ± 3.521.13 ± 3.03
PrimaryCD16/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
24 hours after ECMO commencement
Reported as:
Mean · percentage change
CD16/41
percentage change7+ Days<7 Days
CD16/413.11 ± 1.90.64 ± 3.26
PrimaryCD16/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
48 hours after ECMO commencement
Reported as:
Mean · percentage change
CD16/41
percentage change7+ Days<7 Days
CD16/410.73 ± 3.860.4 ± 4.3
PrimaryCD16/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
72 hours after ECMO commencement
Reported as:
Mean · percentage change
CD16/41
percentage change7+ Days<7 Days
CD16/411.55 ± 3.370.93 ± 1.99
PrimaryCD16/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
24 hours after decannulation
Reported as:
Mean · percentage change
CD16/41
percentage change7+ Days<7 Days
CD16/411.56 ± 2.270.6 ± 3.98
PrimaryCD14/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
12 hours after ECMO commencement
Reported as:
Mean · percentage change
CD14/41
percentage change7+ Days<7 Days
CD14/411.5 ± 3.370.84 ± 2.97
PrimaryCD14/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
24 hours after ECMO commencement
Reported as:
Mean · percentage change
CD14/41
percentage change7+ Days<7 Days
CD14/413.02 ± 2.390.38 ± 3.48
PrimaryCD14/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
48 hours after ECMO commencement
Reported as:
Mean · percentage change
CD14/41
percentage change7+ Days<7 Days
CD14/410.29 ± 4.510.27 ± 5.78
PrimaryCD14/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
72 hours after ECMO commencement
Reported as:
Mean · percentage change
CD14/41
percentage change7+ Days<7 Days
CD14/410.72 ± 4.650.59 ± 2.73
PrimaryCD14/41

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
24 hours after ECMO decannulation
Reported as:
Mean · percentage change
CD14/41
percentage change7+ Days<7 Days
CD14/411.01 ± 3.030.40 ± 4.58
PrimaryCD64/163

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
12 hours after ECMO commencement
Reported as:
Mean · percentage change
CD64/163
percentage change7+ Days<7 Days
CD64/1638.7 ± 2.524.65 ± 2.81
PrimaryCD64/163

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
24 hours after ECMO commencement
Reported as:
Mean · percentage change
CD64/163
percentage change7+ Days<7 Days
CD64/1637.34 ± 5.131.89 ± 5.87
PrimaryCD64/163

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
48 hours after ECMO commencement
Reported as:
Mean · percentage change
CD64/163
percentage change7+ Days<7 Days
CD64/1633.26 ± 4.150.92 ± 2.52
PrimaryCD64/163

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
72 hours after ECMO commencement
Reported as:
Mean · percentage change
CD64/163
percentage change7+ Days<7 Days
CD64/1633.31 ± 3.391.9 ± 3.86
PrimaryCD64/163

Change of markers of platelet and leukocyte activation in arterial blood and analysed by flow cytometry.

Time frame:
24 hours after decannulation
Reported as:
Mean · percentage change
CD64/163
percentage change7+ Days<7 Days
CD64/1633.2 ± 3.552.27 ± 2.89
SecondaryChange of Serum Haemoglobin Levels

Clinical and biochemical markers of organ failure

Time frame:
baseline
Reported as:
Mean · g/L
Change of Serum Haemoglobin Levels
g/L7+ Days<7 Days
Change of Serum Haemoglobin Levels151.5 ± 33.0145.4 ± 41.5
SecondaryDuration on ECMO

Clinical and biochemical markers of organ failure

Time frame:
> 7 days or did not survive to discharge
Reported as:
Median · hours
Duration on ECMO
hours7+ Days<7 Days
Duration on ECMO292 (186 to 360)80 (59 to 91)
SecondaryNumber of Participants With Acute Kidney Injury

Clinical and biochemical markers of organ failure

Time frame:
>7 days or did not survive to discharge
Reported as:
Number · participants
Number of Participants With Acute Kidney Injury
participants7+ Days<7 Days
Number of Participants With Acute Kidney Injury30
SecondaryHeart Injury as Determined by Serum Troponin Levels

Clinical and biochemical markers of organ failure

Time frame:
12 hours after ECMO commencement
Reported as:
Mean · ng/ml
Heart Injury as Determined by Serum Troponin Levels
ng/ml7+ Days<7 Days
Heart Injury as Determined by Serum Troponin Levels7.89 ± 1.176.96 ± 1.14
SecondaryAllogenic Red Cell Transfusion Volume

Clinical and biochemical markers of organ failure

Time frame:
24 hours after ECMO is discontinued
Reported as:
Mean · ml
Allogenic Red Cell Transfusion Volume
ml7+ Days<7 Days
Allogenic Red Cell Transfusion Volume289.6 ± 241.0479.2 ± 268.2
SecondaryNumber of Participants Requiring Non Red Cell Transfusion

Clinical and biochemical markers of organ failure

Time frame:
24 hours after ECMO is discontinued
Reported as:
Count of participants · Participants
Number of Participants Requiring Non Red Cell Transfusion
Participants7+ Days<7 Days
Number of Participants Requiring Non Red Cell Transfusion1010
SecondaryHeart Injury as Determined by Serum Troponin Levels

Clinical and biochemical markers of organ failure

Time frame:
24 hours after ECMO commencement
Reported as:
Mean · ng/ml
Heart Injury as Determined by Serum Troponin Levels
ng/ml7+ Days<7 Days
Heart Injury as Determined by Serum Troponin Levels3.71 ± 1.543.11 ± 1.62
SecondaryHeart Injury as Determined by Serum Troponin Levels

Clinical and biochemical markers of organ failure

Time frame:
48 hours after ECMO commencement
Reported as:
Mean · ng/ml
Heart Injury as Determined by Serum Troponin Levels
ng/ml7+ Days<7 Days
Heart Injury as Determined by Serum Troponin Levels2.13 ± 1.141.81 ± 1.28
SecondaryHeart Injury as Determined by Serum Troponin Levels

Clinical and biochemical markers of organ failure

Time frame:
72 hours after ECMO commencement
Reported as:
Mean · ng/ml
Heart Injury as Determined by Serum Troponin Levels
ng/ml7+ Days<7 Days
Heart Injury as Determined by Serum Troponin Levels5.51 ± 2.035.88 ± 2.09
SecondaryHeart Injury as Determined by Serum Troponin Levels

Clinical and biochemical markers of organ failure

Time frame:
24 hours after decannulation
Reported as:
Mean · ng/ml
Heart Injury as Determined by Serum Troponin Levels
ng/ml7+ Days<7 Days
Heart Injury as Determined by Serum Troponin Levels9.54 ± 1.397.44 ± 1.41
SecondaryChange of Serum Haemoglobin Levels

Clinical and biochemical markers of organ failure

Time frame:
12 hours after ECMO commencement
Reported as:
Mean · g/L
Change of Serum Haemoglobin Levels
g/L7+ Days<7 Days
Change of Serum Haemoglobin Levels109.64 ± 20.81112.07 ± 16.33
SecondaryChange of Serum Haemoglobin Levels

Clinical and biochemical markers of organ failure

Time frame:
24 hours after ECMO commencement
Reported as:
Mean · g/L
Change of Serum Haemoglobin Levels
g/L7+ Days<7 Days
Change of Serum Haemoglobin Levels114.30 ± 11.92109.43 ± 24.52
SecondaryChange of Serum Haemoglobin Levels

Clinical and biochemical markers of organ failure

Time frame:
48 hours after ECMO commencement
Reported as:
Mean · g/L
Change of Serum Haemoglobin Levels
g/L7+ Days<7 Days
Change of Serum Haemoglobin Levels112.56 ± 9.14113.08 ± 6.32
SecondaryChange of Serum Haemoglobin Levels

Clinical and biochemical markers of organ failure

Time frame:
72 hours after ECMO commencement
Reported as:
Mean · g/L
Change of Serum Haemoglobin Levels
g/L7+ Days<7 Days
Change of Serum Haemoglobin Levels112.90 ± 7.65109.89 ± 3.79
SecondaryChange of Serum Haemoglobin Levels

Clinical and biochemical markers of organ failure

Time frame:
24 hours after decannulation
Reported as:
Mean · g/L
Change of Serum Haemoglobin Levels
g/L7+ Days<7 Days
Change of Serum Haemoglobin Levels109.25 ± 11.44110.23 ± 12.15

Adverse events

Collected over Until discharge from Hospital. Non-serious events are listed at a 0% frequency threshold.

Adverse event summary by group
GroupDeathsSeriousOther
1 - Observational Case-Controls3/24 (12.5%)3/24 (12.5%)1/24 (4.2%)
Most frequent serious events
Most frequent serious events
Event1 - Observational Case-Controls
FatalCongenital, familial and genetic disorders1/24
FatalCongenital, familial and genetic disorders1/24
FatalCongenital, familial and genetic disorders1/24
Most frequent other events
Most frequent other events
Event1 - Observational Case-Controls
ResolvedCongenital, familial and genetic disorders1/24

Baseline characteristics

Age, Categorical
Age, Categorical(Participants)1 - Observational Case-Controls
<=18 years24
Between 18 and 65 years0
>=65 years0
Sex: Female, Male
Sex: Female, Male(Participants)1 - Observational Case-Controls
Female11
Male13
Ethnicity (NIH/OMB)
Ethnicity (NIH/OMB)(Participants)1 - Observational Case-Controls
Hispanic or Latino0
Not Hispanic or Latino24
Unknown or Not Reported0
Gestational age
Gestational age(weeks)1 - Observational Case-Controls
Mean40.6 ± 2.6
Weight at birth
Weight at birth(kilograms)1 - Observational Case-Controls
Mean3.2 (2.9 to 3.5)
08

Study locations

1 site
  • University Hospitals of Leicester NHS Trust
    Leicester, LE3 9QP, United Kingdom
09

References and documents

Publications

  • Mamikonian LS, Mamo LB, Smith PB, Koo J, Lodge AJ, Turi JL. Cardiopulmonary bypass is associated with hemolysis and acute kidney injury in neonates, infants, and children*. Pediatr Crit Care Med. 2014 Mar;15(3):e111-9. doi: 10.1097/PCC.0000000000000047. PubMed 24394997 ↗
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  • Mugford M, Elbourne D, Field D. Extracorporeal membrane oxygenation for severe respiratory failure in newborn infants. Cochrane Database Syst Rev. 2008 Jul 16;(3):CD001340. doi: 10.1002/14651858.CD001340.pub2. PubMed 18646070 ↗
  • Konduri GG, Kim UO. Advances in the diagnosis and management of persistent pulmonary hypertension of the newborn. Pediatr Clin North Am. 2009 Jun;56(3):579-600, Table of Contents. doi: 10.1016/j.pcl.2009.04.004. PubMed 19501693 ↗
  • Bahrami KR, Van Meurs KP. ECMO for neonatal respiratory failure. Semin Perinatol. 2005 Feb;29(1):15-23. doi: 10.1053/j.semperi.2005.02.004. PubMed 15921148 ↗
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  • Lazar DA, Cass DL, Olutoye OO, Welty SE, Fernandes CJ, Rycus PT, Lee TC. The use of ECMO for persistent pulmonary hypertension of the newborn: a decade of experience. J Surg Res. 2012 Oct;177(2):263-7. doi: 10.1016/j.jss.2012.07.058. Epub 2012 Aug 10. PubMed 22901797 ↗
  • McNally H, Bennett CC, Elbourne D, Field DJ; UK Collaborative ECMO Trial Group. United Kingdom collaborative randomized trial of neonatal extracorporeal membrane oxygenation: follow-up to age 7 years. Pediatrics. 2006 May;117(5):e845-54. doi: 10.1542/peds.2005-1167. Epub 2006 Apr 24. PubMed 16636114 ↗
  • Farrow KN, Fliman P, Steinhorn RH. The diseases treated with ECMO: focus on PPHN. Semin Perinatol. 2005 Feb;29(1):8-14. doi: 10.1053/j.semperi.2005.02.003. PubMed 15921147 ↗
  • Bendapudi P, Rao GG, Greenough A. Diagnosis and management of persistent pulmonary hypertension of the newborn. Paediatr Respir Rev. 2015 Jun;16(3):157-61. doi: 10.1016/j.prrv.2015.02.001. Epub 2015 Feb 10. PubMed 25765845 ↗
  • Puthiyachirakkal M, Mhanna MJ. Pathophysiology, management, and outcome of persistent pulmonary hypertension of the newborn: a clinical review. Front Pediatr. 2013 Sep 2;1:23. doi: 10.3389/fped.2013.00023. PubMed 24400269 ↗
  • McILwain RB, Timpa JG, Kurundkar AR, Holt DW, Kelly DR, Hartman YE, Neel ML, Karnatak RK, Schelonka RL, Anantharamaiah GM, Killingsworth CR, Maheshwari A. Plasma concentrations of inflammatory cytokines rise rapidly during ECMO-related SIRS due to the release of preformed stores in the intestine. Lab Invest. 2010 Jan;90(1):128-39. doi: 10.1038/labinvest.2009.119. Epub 2009 Nov 9. PubMed 19901912 ↗
  • Fortenberry JD, Bhardwaj V, Niemer P, Cornish JD, Wright JA, Bland L. Neutrophil and cytokine activation with neonatal extracorporeal membrane oxygenation. J Pediatr. 1996 May;128(5 Pt 1):670-8. doi: 10.1016/s0022-3476(96)80133-8. PubMed 8627440 ↗
  • Mildner RJ, Taub N, Vyas JR, Killer HM, Firmin RK, Field DJ, Kotecha S. Cytokine imbalance in infants receiving extracorporeal membrane oxygenation for respiratory failure. Biol Neonate. 2005;88(4):321-7. doi: 10.1159/000087630. Epub 2005 Aug 18. PubMed 16113527 ↗
  • Graulich J, Walzog B, Marcinkowski M, Bauer K, Kossel H, Fuhrmann G, Buhrer C, Gaehtgens P, Versmold HT. Leukocyte and endothelial activation in a laboratory model of extracorporeal membrane oxygenation (ECMO). Pediatr Res. 2000 Nov;48(5):679-84. doi: 10.1203/00006450-200011000-00021. PubMed 11044491 ↗
  • Golej J, Winter P, Schoffmann G, Kahlbacher H, Stoll E, Boigner H, Trittenwein G. Impact of extracorporeal membrane oxygenation modality on cytokine release during rescue from infant hypoxia. Shock. 2003 Aug;20(2):110-5. doi: 10.1097/01.shk.0000075571.93053.2c. PubMed 12865653 ↗
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  • Kozik DJ, Tweddell JS. Characterizing the inflammatory response to cardiopulmonary bypass in children. Ann Thorac Surg. 2006 Jun;81(6):S2347-54. doi: 10.1016/j.athoracsur.2006.02.073. PubMed 16731102 ↗
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  • Warren OJ, Smith AJ, Alexiou C, Rogers PL, Jawad N, Vincent C, Darzi AW, Athanasiou T. The inflammatory response to cardiopulmonary bypass: part 1--mechanisms of pathogenesis. J Cardiothorac Vasc Anesth. 2009 Apr;23(2):223-31. doi: 10.1053/j.jvca.2008.08.007. Epub 2008 Oct 19. No abstract available. PubMed 18930659 ↗
  • Warren OJ, Watret AL, de Wit KL, Alexiou C, Vincent C, Darzi AW, Athanasiou T. The inflammatory response to cardiopulmonary bypass: part 2--anti-inflammatory therapeutic strategies. J Cardiothorac Vasc Anesth. 2009 Jun;23(3):384-93. doi: 10.1053/j.jvca.2008.09.007. Epub 2008 Dec 3. No abstract available. PubMed 19054695 ↗
  • Williams DC, Turi JL, Hornik CP, Bonadonna DK, Williford WL, Walczak RJ, Watt KM, Cheifetz IM. Circuit oxygenator contributes to extracorporeal membrane oxygenation-induced hemolysis. ASAIO J. 2015 Mar-Apr;61(2):190-5. doi: 10.1097/MAT.0000000000000173. PubMed 25419829 ↗
  • Omar HR, Mirsaeidi M, Socias S, Sprenker C, Caldeira C, Camporesi EM, Mangar D. Plasma Free Hemoglobin Is an Independent Predictor of Mortality among Patients on Extracorporeal Membrane Oxygenation Support. PLoS One. 2015 Apr 22;10(4):e0124034. doi: 10.1371/journal.pone.0124034. eCollection 2015. PubMed 25902047 ↗
  • Lou S, MacLaren G, Best D, Delzoppo C, Butt W. Hemolysis in pediatric patients receiving centrifugal-pump extracorporeal membrane oxygenation: prevalence, risk factors, and outcomes. Crit Care Med. 2014 May;42(5):1213-20. doi: 10.1097/CCM.0000000000000128. PubMed 24351369 ↗
  • Lubnow M, Philipp A, Foltan M, Bull Enger T, Lunz D, Bein T, Haneya A, Schmid C, Riegger G, Muller T, Lehle K. Technical complications during veno-venous extracorporeal membrane oxygenation and their relevance predicting a system-exchange--retrospective analysis of 265 cases. PLoS One. 2014 Dec 2;9(12):e112316. doi: 10.1371/journal.pone.0112316. eCollection 2014. PubMed 25464516 ↗
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Study documents

  • Study protocol · Feb 27, 2017
  • Statistical analysis plan · May 1, 2018

Documents are hosted by the registry — open the source record to download them.

Individual participant data

Plan to share: Yes — statistical analysis

10

Updates

Tracking since Sep 25, 2026
No changes since tracking began. The registry record was last updated on Mar 19, 2020, before this site started recording changes on Sep 25, 2026. Its history is on ClinicalTrials.gov ↗
11

Registry details

Key details

Study ID
NCT02940327
Lead sponsor
University of Leicester
Collaborators
University Hospitals, Leicester, Heart Link Children's Charity, British Heart Foundation
Responsible party
Sponsor
First posted
Oct 20, 2016
Start date
Feb 19, 2016
Primary completion
Jul 10, 2017
Completion
Jul 10, 2017
Results posted
Mar 19, 2020
Last update
Mar 19, 2020

Oversight

Data monitoring committee
No
View the source record on ClinicalTrials.gov ↗

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